One method of treating circulatory disorders has been to provide pumping assistance devices attempt to provide a non-invasive procedure for safely and effectively applying pressure to specific parts of the body. External counter pulsation devices or “ECP” devices were introduced as non-invasive circulatory assistance devices by moving blood from the extremities (legs and buttocks) up to the heart to treat angina pectoris, acute myocardial infarctions (heart attacks) and cardiogenic shock. The early ECP devices employed a liquid, typically water, to compress the extremities. Later ECP devices employed air to compress the extremities, which avoided the need to heat the water to body temperature and the risk of an electrical shock if a balloon or bladder containing the water were to leak or burst, such early ECP devices are disclosed in U.S. Pat. Nos. 3,288,132, 3,303,841, 3,403,673, 3,734,087, 3,835,845, 3,654,919, 3,866,604 and 3,388,919. Such devices are seen in FIG. 1 and show the four steps in compression. Current ECP devices typically include bladders disposed in pockets within each of two pairs of cuffs, which are fastened about the calves and thighs of a person, and two bladders contained in a single cuff which is fastened about his or her buttocks as shown in FIG. 1.
A controller operates the actuation of a plurality of valves, which valves are mounted in communication with a plurality of individual inflatable cuffs encasing the calves, thighs, and buttocks in any desired sequence towards the heart during diastole or systole, at desired times during the cardiac. A cycle of selected duration and pressures is employed for treating a variety of cardiac and non-cardiac circulatory conditions.
Another method of treating circulatory and related illness is the use of compositions which can include various drug and/or nutrients and micronutrients to improve symptoms or outcomes in chronic illness. Limited data on the actions of individual agents both in-vitro, in-vivo or in animal studies exist as to such nutrient treatments.
Unfortunately, treatments of disease processes tend to revert to the observable physiologic changes back toward a normalized condition similar to the observable, original homeostatic condition. Correction of these end-effects usually leaves the underlying molecular rearrangements responsible for the physiologic change unaffected. Treatment of vasoconstriction for example, uses vasodilators leaving the original molecular cause of the vasoconstriction untreated. The untreated molecular rearrangement processes responsible for the vasoconstriction continue unabated with resulting molecular effects which are now known to include transcriptional processes, calcium release, mitogenic effects, smooth muscle hypertrophy, autocrine and paracrine effects, and extracellular matrix accumulation of peptides all of which are both catalytic and space occupying properties.
Accumulative research evidence over the past decades indicates that molecular actions in cellular physiology are all pleuripotential, sensitive in their context sensitive as well as modifiable by numerous concurrent molecular processes. The order and organization of molecular processes in cells is highly regulated by concurrent reactions and activities in the contiguous milieu of reactants. Phosphorylation-dephosphorylation regulated processes, redox paired reactions, calcium release calmodulin activated enzyme reactions with a host of signaling transcription processes remaining tightly regulated by concurrent reaction pathways with interregulated functions.
There is an understanding that the endothelial inner lining layer of the circulatory system and other parts of the body play a major role in health and disease through responses to shear stress from circulating fluids flowing across it or pulsating upon it. The recognition that vascular endothelium is a highly active metabolic organ came with the discovery that it actively liberated nitric oxide (i.e., a mediator, a powerful relaxant of vascular smooth muscle as a function of shear stress and pulse frequency across the endothelial surface). There are known beneficial effects of provided by mediators, but there has yet to be a highly suitable means for obtaining a desired balance in the vascular system. Attempts to directly administer nitric oxide do not appear to result in a highly useful mediator due to competing molecular reactions potential toxicity. Thus, efforts to find ways to naturally release mediators into the vascular system appear to be the most feasible solution. Compounds such as nitroglycerin and other organic nitrate compounds release nitric oxide through enzymatic degradation and act directly on vascular smooth muscle to cause vasodilation. These compounds are designated endothelium independent vasodilators since they relax vascular smooth muscle even though vascular endothelium may be dysfunctional or destroyed at a given site of action. Nitric oxide donors raise a number of issues for competing metabolic events.
In addition, the present invention provides for a treatment addressing control of high concentrations of C-reactive protein (CRP) which can produce the following cascade of pathophysiological events leading toward the development of cornary vascular disease. CRP is thought to: promote monocyte chemotaxis, facilitates low-density lipoprotein uptake by macrophages in vitro; increase angiotensin type I receptor numbers and angiotensin type I receptor mediated reactive oxygen species formation, in vascular smooth muscle cells; activate stress-activated protein kinases p38 kinase and c-Jun N-terminal kinase (JNK); facilitate the release of plasminogen activator inhibitor- and endothelin-1, increase the expression of cell adhesion molecules, reduce NO bioavailability and provides the mechanism responsible for the reduced NO bioavailability in increased vascular oxidative stress; increase the production of superoxide, an NO scavenger, in cultured human aortic endothelial cells; increase oxidative stress and reduce NO bioavailability in the systemic circulation of patients with coronary artery disease; directly influence NO-mediated function by increasing oxidative stress in the coronary circulation since coronary arterioles are the predominant vessels regulating blood flow in the heart; CRP at concentrations known to predict future vascular events, weakens the antioxidant defenses of endothelial progenitor cells, and promotes early senescence through telomerase; and CRP treated cultured cells causes a significant increase in vascular NADPH oxidase activity. NADPH oxidase is a major source of agonist-induced superoxide production in vascular cells.
The prior art provided treatments for such circulatory disorders with some success. However, there remains a need to improve upon the art. The present invention provides an enhanced system for treating circulatory systems.